Comparison of Catecholamine Values Before and After Exercise-Induced Bronchospasm in Professional Cyclists.

Background
The concentration of circulating catecholamine increases during exercise in healthy athletes, but the variation has not been studied much in athletes who develop exercise-induced bronchospasm. This study measured changes in circulating catecholamine levels using the induced maximal effort test in the laboratory in professional cyclists sensitive to bronchospasm.


Materials and Methods
This experimental study included 86 professional cyclists. They underwent two pulmonary function tests (to determine forced expiratory volume in one second [FEV1]) and two blood samples (to measure adrenaline and noradrenaline levels) were drawn before and after the stress test. Two subsets emerged: subjects whose FEV1 decreased by at least 10% from the resting value and non-sensitive subjects whose FEV1 do not meet this criterion.


Results
A total of 51 cyclists (59%) were classified into the sensitive group. Resting catecholamine levels showed no significant difference (p > 0.05) between the two groups. In contrast, at the end of the exercise test, the adrenaline (581.9 ± 321.0 pg/mL versus 1783.5 ± 1001.0 pg/mL) and noradrenaline (4994.0 ± 2373.0 pg/mL versus 3205.0 ± 7714.4 pg/mL) levels were both lower in the sensitive group than those in the resting group (p < 0.0001).


Conclusion
The frequency of the occurrence of bronchospasm observed in the studied cyclists was one of the highest among professional sports environments and the circulating catecholamine level was low in cyclists susceptible to bronchospasm. A training protocol adapted to their respiratory physiological profile may be indicated.


INTRODUCTION
Catecholamine is derived from amino acids such as adrenaline and noradrenaline, which are also major components. Both hormones are synthesized by adrenal medulla cells (1,2). Noradrenaline acts as both a neurotransmitter and a hormone, while adrenaline simply acts as a hormone. Catecholamine acts through membrane receptors (1) and at least two adrenergic receptor sites (α; β), which are divided into two groups: α 1 and α 2 receptors and β 1 , β 2, and β 3 receptors (3,4). Noradrenaline activates α receptors and adrenaline acts on β receptors, although adrenaline can also activate α receptors (5).
Among the sedentary and athletic, catecholamine concentrations are influenced by emotional factors and physical exercise among others. Indeed, exercise, hypoglycemia, and hypoxia are stressful situations that can TANAFFOS Messan F,et al. 137 Tanaffos 2017; 16 (2): [136][137][138][139][140][141][142][143] cause instability in the major functions of organs (6). To restore homeostasis, the nervous and endocrine systems generate potent mediators involved in physiological regulation and, therefore, homeostasis. However, heightened secretion of catecholamine, including that of adrenaline and noradrenaline, occurs in response to exercise (6). Various studies have highlighted the role of catecholamine in the control of functions that affect physical performance and recent studies have focused on the effects induced by the duration and intensity of exercise on sympathoadrenal activity (7,8). We also know that at a constant volume of oxygen consumption, continuous and substantial increases in the concentration of noradrenaline are observed in athletes (9)(10)(11). Even at very low-intensity exertion, increased adrenaline and noradrenaline concentrations are observed; however, the noradrenaline increase occurs faster than that of adrenaline (12). Increasing catecholamine concentrations are relatively more sensitive to high intensities that maximal aerobic power (13)(14)(15)(16)(17)(18)(19)(20)(21)(22). For example, in training and in competition, professional cyclists are faced with high levels of intensity and exposure to air pollutants. Indeed, these cyclists are subject to a training volume of 30 hours per week and a maximum oxygen consumption of approximately 67 mL -1 .kg -1 . They travel more than 4,000 km of road per year and are most often exposed to air pollutants. The significant volume of air commonly ventilated by professional cyclists in adverse environmental and climatic conditions is likely to cause respiratory airway damage. Additionally, microcracks generated by hyperventilation cause cellular permeability to Na + , Cl -, K + , and Ca 2+ . They induce the release of chemical mediators involved in the initial inflammatory process-induced bronchospasm of exercise.
Hyperventilation in a polluted atmosphere is detrimental to the lung function of these cyclists, leading to ventilator disorders and an increased asthma prevalence from 48 % to 55 % has been reported in athletes (23)(24)(25)(26)(27)(28). Physical exercise and sports training impose stress to the central nervous system that subsequently triggers two feedback loops in the hypothalamus and the adrenal medulla, generating acetylcholine and catecholamine, respectively.
Catecholamine contributes to smooth muscle relaxation and inhibition of the release of mediators of inflammation by binding to mast cell receptors, preventing their bridging. As exercise-induced bronchospasm (EIB) is characterized by respiratory airway resistance and the flow of inspired air, it is reasonable to hypothesize that, in susceptible athletes with exercise-induced bronchospasm, the concentration of catecholamine at the end of physical exertion is lower than that in non-sensitive athletes.
Therefore, to test this hypothesis, this study was conducted among professional cyclists with the following aims: 1) diagnose EIB and 2) compare the postexercise concentrations of catecholamine in subjects who are sensitive and non-sensitive to EIB.

Experimental Design
The study sample comprised 86 male professional cyclists aged 19 to 33 years whose anthropometric characteristics are presented in Table 1

Measurement of catecholamine levels
The noradrenaline and adrenaline concentrations were

Study variables
The

Statistical analysis
The anthropometric values of the EIB (+) and EIB (-) groups were compared using unpaired Student's t-tests.
Similarly, the catecholamine concentrations observed at rest and at late efforts were compared to each modality between the two groups using a two-way analysis of variance (ANOVA) (for interaction EIB status x time of measurement), followed by unpaired Student's t-tests. The

Features of the studied cyclists
The characteristics of the subjects are presented in  untrained subjects. Moreover, Caillaud et al. (32) showed that a minimal exercise time was required to induce an increase in catecholamine, even at high intensity. However, this hypothesis has not been not confirmed because the study methods differ from each other (16,22,33). In fact, the results of the present work suggest that adrenaline and noradrenaline concentrations are more sensitive to exercise intensity (34)(35)(36). Similarly, noradrenaline concentration increases exponentially with exercise intensity (37,38).
Kajaer et al. (39) showed that plasma noradrenaline is sensitive to an increase after 60 minutes of exercise when performed at 35% of VO 2max compared to 20 minutes of exercise performed at 40-50% of VO 2max and that the increase occurs prior to an increase in adrenaline concentration. Based on work by Zouhal (6), the sensitivity to increased plasma concentrations of adrenaline and noradrenaline, although linked to a rise in VO 2max and heart rate, seems to be higher after a year of isometric and dynamic exercise. Similarly, the time duration that the subjects are observed prior to blood sampling may be a variable factor. For example, after brief and intense exercise, Hagberg et al. (40) showed that the concentrations of catecholamine quickly return to their baseline values and even fall by 35% after one minute of rest (38,41).